Seoul National University · 医学
Professor Jong-Ho Lee's research lab focuses on the intersection of cancer metabolism and nanomaterials for regenerative medicine. The lab investigates metabolic reprogramming in cancer, particularly the role of key glycolytic enzymes like PFKP in glioblastoma, and explores how signaling pathways such as PI3K/AKT regulate tumor progression. Concurrently, the lab develops advanced graphene-based nanocomposites—such as rGO/HAp hybrids—to enhance osteogenic differentiation of stem cells and promote bone regeneration, demonstrating their potential as bioactive materials in tissue engineering. These dual research directions highlight a strong emphasis on translational applications in oncology and regenerative medicine.
Figures are computed from collected data and may differ slightly.
Phosphofructokinase 1 (PFK1) plays a critical role in glycolysis; however, its role and regulation in tumorigenesis are not well understood. Here, we demonstrate that PFK1 platelet isoform (PFKP) is the predominant PFK1 isoform in human glioblastoma cells and its expression correlates with total PFK activity. We show that PFKP is overexpressed in human glioblastoma specimens due to an increased stability, which is induced by AKT activation resulting from phosphatase and tensin homologue (PTEN) l
Recently, graphene-based nanomaterials, in the form of two dimensional substrates or three dimensional foams, have attracted considerable attention as bioactive scaffolds to promote the differentiation of various stem cells towards specific lineages. On the other hand, the potential advantages of using graphene-based hybrid composites directly as factors inducing cellular differentiation as well as tissue regeneration are unclear. This study examined whether nanocomposites of reduced graphene ox
Reduced graphene oxide-coated hydroxyapatite (rGO-coated HAp) composites stimulated the spontaneous osteogenesis in human mesenchymal stem cells in the absence of osteoinductive agents.
Amplification of the chemokines CXCL10 and RANKL has been suggested to promote osteoclast differentiation and osteolytic bone metastasis, but a function for endogenous CXCL10 in these processes is not well established. In this study, we show that endogenous CXCL10 is critical to recruit cancer cells to bone, support osteoclast differentiation and promote for the formation of osteolytic bone metastases. Neutralizing CXCL10 antibody reduced migration of cancer cells expressing the CXCL10 receptor
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